José F. Rodríguez
Group Leader
Research summary
Our main virus model is the infectious bursal disease virus (IBDV), the etiological agent of an acute immunosuppressive disease affecting domestic chickens. Our group is mainly interested in birnavirus structure and morphogenesis; and in the molecular basis for IBDV virulence.
Publications
Lago M, Rodríguez JF, Bandín I, Dopazo CP. Aquabirnavirus polyploidy: A new strategy to modulate virulence? J Gen Virol 2016; 97:1168-1177
Landajuela A, Hervás JH, Antón Z, Montes LR, Gil D, Valle M, Rodriguez JF, Goñi FM, Alonso A. Lipid geometry and bilayer curvature modulate LC3/GABARAP-mediated model autophagosomal elongation. Biophys J 2016; 110: 411-22
Ferrero D, Garriga D, Navarro A, Rodríguez JF, Verdaguer N. Infectious bursal disease virus VP3 upregulates VP1-mediated RNA-dependent RNA replication. J Virol 2015; 89: 11165-8
Méndez F, de Garay T, Rodríguez D, Rodríguez JF. Infectious bursal disease virus VP5 polypeptide: a phosphoinositide-binding protein required for efficient cell-to-cell virus dissemination. PLoS One 2015; 10: e0123470
Ferrero DS, Buxaderas M, Rodríguez JF, Verdaguer N. The structure of the RNA-dependent RNA polymerase of a permutotetravirus suggests a link between primer-dependent and primer-independent polymerases. PLoS Pathog 2015; 11: e1005265
The Birnaviridae family comprises naked icosahedral viruses with bipartite dsRNA genomes that infect a wide variety of animal species including insects, aquatic fauna and birds. Despite its socioeconomic importance, critical aspects of birnavirus molecular biology are poorly characterized. Our main virus model, infectious bursal disease virus (IBDV), is the aetiological agent of an acute immunosuppressive disease that affects juvenile domestic chickens and causes heavy economic losses to the poultry industry world-wide (http://www.oie.int/eng/maladies/en_classification2007.htm?e1d7). The main goal of our laboratory is to better understand the virus-host interactions that underlie birnavirus pathogenesis, and to use this knowledge to develop sustainable strategies for birnavirus-borne disease control.
Our group currently focuses on unravelling the strategies the virus uses to evade host innate immune responses and on characterizing virus egress mechanism(s) and their relation to virus virulence.
We recently showed that VP3 polypeptide, a dsRNA binding protein, acts as an efficient sheltering device that prevents detection of virus replication complexes by specialised cell sensors, thus preventing the onset of specific antiviral responses. By mapping the VP3-dsRNA binding domain, we determined that single mutations that affect a critical lysine residue within this domain are sufficient to completely abrogate virus replication.
The release of IBDV particles is customarily viewed as a process directly linked to the destruction of infected cells. Recent data from our laboratory nonetheless strongly suggest that IBDV also uses an alternative non-lytic cell-to-cell spreading mechanism. This mechanism appears to be strictly dependent on expression of VP5, a small, non-structural virus polypeptide that specifically binds monophosphorylated phosphoinositide lipids found at the cytosolic face of distinct cell membranes. Characterisation of this alternative egress mechanism could offer new prospects for efficient control of IBDV dissemination.
